TY - JOUR
T1 - A Qrr noncoding RNA deploys four different regulatory mechanisms to optimize quorum-sensing dynamics
AU - Feng, Lihui
AU - Rutherford, Steven T.
AU - Papenfort, Kai
AU - Bagert, John D.
AU - Van Kessel, Julia C.
AU - Tirrell, David A.
AU - Wingreen, Ned S.
AU - Bassler, Bonnie Lynn
N1 - Funding Information:
We thank Terence Hwa for generously providing the BW-RI strain and the pZA31-lucNB and pZE12G plasmids. We are indebted to members of the B.L.B. and N.S.W. laboratories for insightful discussions and suggestions. This work was supported by the Howard Hughes Medical Institute, NIH grant 5R01GM065859 and National Science Foundation (NSF) grant MCB-0343821 to B.L.B., NIH grant R01GM082938 to N.S.W., and NIH grant R01GM062523 and the Institute for Collaborative Biotechnologies through grant W911NF-09-0001 from the U.S. Army Research Office to D.A.T. K.P. is supported by a postdoctoral fellowship from the Human Frontiers in Science Program (HFSP). S.T.R. was supported by NIH fellowship F32AI085922. J.C.V.K. is supported by funds from Indiana University.
Publisher Copyright:
© 2015 Elsevier Inc.
PY - 2015/1/15
Y1 - 2015/1/15
N2 - Quorum sensing is a cell-cell communication process that bacteria use to transition between individual and social lifestyles. In vibrios, homologous small RNAs called the Qrr sRNAs function at the center of quorum-sensing pathways. The Qrr sRNAs regulate multiple mRNA targets including those encoding the quorum-sensing regulatory components luxR, luxO, luxM, and aphA. We show that a representative Qrr, Qrr3, uses four distinct mechanisms to control its particular targets: the Qrr3 sRNA represses luxR through catalytic degradation, represses luxM through coupled degradation, represses luxO through sequestration, and activates aphA by revealing the ribosome binding site while the sRNA itself is degraded. Qrr3 forms different base-pairing interactions with each mRNA target, and the particular pairing strategy determines which regulatory mechanism occurs. Combined mathematical modeling and experiments show that the specific Qrr regulatory mechanism employed governs the potency, dynamics, and competition of target mRNA regulation, which in turn, defines the overall quorum-sensing response.
AB - Quorum sensing is a cell-cell communication process that bacteria use to transition between individual and social lifestyles. In vibrios, homologous small RNAs called the Qrr sRNAs function at the center of quorum-sensing pathways. The Qrr sRNAs regulate multiple mRNA targets including those encoding the quorum-sensing regulatory components luxR, luxO, luxM, and aphA. We show that a representative Qrr, Qrr3, uses four distinct mechanisms to control its particular targets: the Qrr3 sRNA represses luxR through catalytic degradation, represses luxM through coupled degradation, represses luxO through sequestration, and activates aphA by revealing the ribosome binding site while the sRNA itself is degraded. Qrr3 forms different base-pairing interactions with each mRNA target, and the particular pairing strategy determines which regulatory mechanism occurs. Combined mathematical modeling and experiments show that the specific Qrr regulatory mechanism employed governs the potency, dynamics, and competition of target mRNA regulation, which in turn, defines the overall quorum-sensing response.
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U2 - 10.1016/j.cell.2014.11.051
DO - 10.1016/j.cell.2014.11.051
M3 - Article
C2 - 25579683
AN - SCOPUS:84920992591
SN - 0092-8674
VL - 160
SP - 228
EP - 240
JO - Cell
JF - Cell
IS - 1-2
ER -